By tracing the transcriptomes of neurons that wither early and late in the course of Alzheimer’s disease, researchers peg subpopulations of excitatory neurons in entorhinal cortex as selectively vulnerable to tau. Reactive astrocytes aid and abet.
White matter-associated microglia express similar genes to plaque-associated DAMs. They seem to be triggered by the myelin breakdown associated with aging and disease.
The commercial test uses a few drops of saliva. It must be ordered by a physician. Plans are also in the works to use the test to select participants for clinical trials.
Breaking familiar gene-disease patterns, HTT trinucleotide expansions lead to huntingtin aggregates in prefrontal cortex. Noncoding caveolin 1 variants suppress its expression.
This astrocytic glycoprotein greases glial phagocytosis and reduces plaque burden in mice. The circadian clock protein Bmal1 suppresses it.
This pathway may transmogrify microglia during neurodegeneration, without the help of TREM2.
Sensor algorithms can accurately capture patterns of resting tremor and dyskinesia. This could help clinicians manage symptoms and medication.
People who report not participating in social or cognitive activities are more likely to develop dementia within the next few years, but not after that. The findings cast nonparticipation as a consequence, not a cause, of neurodegeneration.
Transcriptomic and epigenomic data pin PD risk genes in GWAS loci; six affect splicing, five expression, four are new.
Two cohorts—IDEAS and WHIMS—show Aβ accumulation and brain shrinkage in cognitively normal and impaired elderly who were exposed to levels of air pollution even within current EPA limits.
Researchers found that bits of tau from the protein’s microtubule-binding region can be detected in the cerebrospinal fluid. These, not phospho-tau or total tau, reflect neurofibrillary tangles in the Alzheimer’s brain.
Confronting unprecedented challenges this past year, scientists found ways to tide their research over and keep clinical trials mostly on track.
In cultured cells, lysosomal activity was necessary to enable tau seeds to break out of internalized exosomes and trigger the aggregation of tau in the cytosol.
Topline results suggested that the anti-inflammatory treatment stabilized cognition and function over six months. The trial did not include biomarkers.
Assays will help doctors diagnose Alzheimer’s disease and amnestic mild cognitive impairment in Taiwanese clinics.